Differential susceptibility hypothesis
According to the differential susceptibility hypothesis by BelskyBelsky 1997b; 1997a; 2005; Belsky & Pluess, 2009 individuals vary in the degree they are affected by environmental, psychological and social factors they are exposed to. Some individuals are more susceptible to such influences than others––not only to negative but also to positive ones. Differential susceptibility versus diathesis-stress The idea that individuals vary in their responsivity to qualities of the environment is generally framed in diathesis-stressMonroe & Simons, 1991; Zuckerman, 1999 or dual-risk terms.Sameroff, 1983 That is, some individuals, due to their biological, temperamental and/or behavioral characteristics (i.e., “diathesis” or “risk 1”), are more vulnerable to the adverse effects of negative experiences (i.e., “stress” or “risk 2”), whereas others are relatively resilient with respect to them (see , an adaptation of Bakermans-Kranenburg and van IJzendoorn’s (2007) Figure 1). A fundamentally different, even if not competing view, of the very same phenomenon is central to Belsky’sBelsky 1997b; 1997a; 2005 differential susceptibility hypothesis and Boyce and Ellis’ (2005) related notion of biological sensitivity to context: Individuals do not simply vary in the degree to which they are vulnerable to the negative effects of adverse experience but, more generally, in their developmental plasticity. More “plastic” or malleable individuals are more susceptible than others to environmental influences in a for-better-and-for-worse manner,Belsky, Bakermans-Kranenburg, & van IJzendoorn, 2007 that is, to both the adverse developmental sequelae associated with negative environments and the positive developmental consequences of supportive ones. Less susceptible individuals, in contrast, are less affected by rearing conditions, be they presumptively supportive or undermining of well being (see Figure 2, an adaptation of Bakermans-Kranenburg and van IJzendoorn’s (2007) Figure 1). Theoretical background of the differential susceptibility hypothesis Because the future is and always has been inherently uncertain, ancestral parents, just like parents today, could not have known (consciously or unconsciously) what childrearing practices would prove most successful in promoting the reproductive fitness of offspring—and thus their own inclusive fitness. As a result, and as a fitness optimizing strategy involving bet hedging,Philipi & Seger, 1989 natural selection would have shaped parents to bear children varying in plasticity.Belsky, 1997a, 2005 This way, if an effect of parenting had proven counterproductive in fitnessterms, those children not affected by parenting would not have incurred the cost of developing in ways that ultimately proved “misguided”. Importantly, in light of inclusive-fitness considerations, these less malleable children’s “resistance” to parental influence would not only have benefited themselves directly, but even their more malleable sibs—indirectly, given that sibs, like parents and children, have 50% of their genes in common. By the same token, had parenting influenced children in ways that enhanced fitness, then not only would more plastic offspring have benefited directly by following parental leads, but so, too, would their parents and even their less malleable sibs who did not benefit from the parenting they received, again for inclusive-fitness reasons. This line of evolutionary argument leads to the prediction that children should vary in their susceptibility to parental rearing and perhaps to environmental influences more generally. As it turns out, a long line of developmental inquiry, informed by a “transactional” perspective,Sameroff, 1983 has more or less been based on this unstated assumption. Criteria for the testing of differential susceptibility Belsky, Bakermans-Kranenburg, & van IJzendoorn, (2007) delineated a series of empirical requirements—or steps—for convincingly establishing evidence of differential susceptibility to environmental influences and distinguishing differential susceptibility from other interaction effects including diathesis-stress/dual-risk. * While diathesis-stress/dual-risk arises when the most vulnerable are disproportionately affected in an adverse manner by a negative environment but do not also benefit disproportionately from positive environmental conditions, differential susceptibility is characterized by a cross-over interaction: the susceptible individuals are disproportionately affected by both negative and positive experiences. * A further criterion that needs to be fulfilled to distinguish differential susceptibility from diathesis-stress/dual-risk is the independence of the outcome measure from the susceptibility factor: if the susceptibility factor and the outcome are related, diathesis-stress/dual-risk is suggested rather than differential susceptibility. * Further, environment and susceptibility factor must also be unrelated to exclude the alternative explanation that susceptibility merely represents a function of the environment. * The specificity of the differential-susceptibility effect is demonstrated if the model is not replicated when other susceptibility factors (i.e., moderators) and outcomes are used. * Finally, the slope for the susceptible subgroup should be significantly different from zero and at the same time significantly steeper than the slope for the non- (or less-) susceptible subgroup. Susceptibility markers and empirical evidence Characteristics of individuals that have been shown to moderate environmental effects in a manner consistent with the differential susceptibility hypothesis can be subdivided into three categoriessee Belsky & Pluess, 2009: # Genetic Factors E.g., Bakermans-Kranenburg and van IJzendoorn (2006) were the first to test the differential susceptibility hypothesis as a function of genes regarding the moderating effect of the dopamine receptor D4 7-repeat polymorphism (DRD4-7R) on the association between maternal sensitivity and externalizing behavior problems in 47 families. Children with the DRD4-7R allele and insensitive mothers displayed significantly more externalizing behaviors than children with the same allele but with sensitive mothers. Children with the DRD4-7R allele and sensitive mothers had the least externalizing behaviors of all whereas maternal sensitivity had no effect on children without the DRD4-7R allele. # Endophenotypic Factors ' E.g., Obradovic, Bush, Stamperdahl, Adler and Boyce’s (2010) investigated associations between childhood adversity and child adjustment in 338 5-year olds. Children with high cortisol reactivity were rated by teachers as least prosocial when living under adverse conditions, but most prosocial when living under more benign conditions (and in comparison to children scoring low on cortisol reactivity). # 'Phenotypic Factors E.g., Pluess and Belsky (2009) reported that the effect of child care quality on teacher-rated socioemotional adjustment varied as a function of infant temperament in the case of 761 4.5-year olds participating in the NICHD Study of Early Child Care and Youth Development (NICHD Early Child Care Research Network, 2005). Children with difficult temperaments as infants manifest the most and least behavior problems depending on whether they experienced, respectively, poor or good quality care (and in comparison to children with easier temperaments). A list of currently proposed susceptibility factors—which all emerged repeatedly in empirical studies—is provided in Table 1. See also * Diathesis-stress model * Endophenotype * Gene-environment interaction * Gene-environment correlation * Genotype * Highly sensitive person * Hypothalamic-pituitary-adrenal axis * Norms of reaction * Phenotype * Resilience * Temperament * Therapygenetics References * Belsky, J. (1997a). Variation in susceptibility to rearing influences: An evolutionary argument. Psychological Inquiry, 8, 182-186. * Belsky, J. (1997b). Theory testing, effect-size evaluation, and differential susceptibility to rearing influence: the case of mothering and attachment. Child Development, 68(4), 598-600. * Belsky, J. (2005). Differential susceptibility to rearing influences: An evolutionary hypothesis and some evidence. In B. Ellis & D. Bjorklund (Eds.), Origins of the social mind: Evolutionary Psychology and Child Development (pp. 139–163). New York: Guildford. * Belsky, J., & Pluess, M. (2009). Beyond Diathesis-Stress: Differential Susceptibility to Environmental Influences. Psychological Bulletin, 135(6), 885-908. * Monroe, S. M., & Simons, A. D. (1991). Diathesis-stress theories in the context of life stress research: implications for the depressive disorders. Psychological Bulletin, 110(3), 406-425. * Zuckerman, M. (1999). Vulnerability to psychopathology: A biosocial model. Washington: American Psychological Association. * Sameroff, A. J. (1983). Developmental systems: Contexts and evolution. In P.Mussen (Ed.), Handbook of child psychology (Vol. 1, pp. 237–294). New York: Wiley. * Boyce, W. T., & Ellis, B. J. (2005). Biological sensitivity to context: I. An evolutionary-developmental theory of the origins and functions of stress reactivity. Development and Psychopathology, 17(2), 271-301. * Bakermans-Kranenburg, M. J., & van IJzendoorn, M. H. (2007). Research Review: genetic vulnerability or differential susceptibility in child development: the case of attachment. Journal of Child Psychology and Psychiatry and Allied Disciplines, 48(12), 1160-1173. * Belsky, J., Bakermans-Kranenburg, M. J., & van IJzendoorn, M. H. (2007). For better and for worse: Differential Susceptibility to environmental influences. Current Directions in Psychological Science, 16(6), 300-304. * Philipi, T., & Seger, J. H. (1989). Hedging evolutionary bets, revisited. TREE, 4, 41-44. * Taylor, S. E., Way, B. M., Welch, W. T., Hilmert, C. J., Lehman, B. J., & Eisenberger, N. I. (2006). Early family environment, current adversity, the serotonin transporter promoter polymorphism, and depressive symptomatology. Biological Psychiatry, 60(7), 671-676. * Obradovic, J., Bush, N. R., Stamperdahl, J., Adler, N. E., & Boyce, W. T. (2010). Biological Sensitivity to Context: The Interactive Effects of Stress Reactivity and Family Adversity on Socio-emotional Behavior and School Readiness. Child Development, 81(1), 270-289. * Pluess, M., & Belsky, J. (2009). Differential Susceptibility to Rearing Experience: The Case of Childcare. Journal of Child Psychology and Psychiatry and Allied Disciplines, 50(4), 396-404. * NICHD Early Child Care Research Network. (2005). Child Care and Child Development: Results of the NICHD Study of Early Child Care and Youth Development. New York: Guilford Press. * Jokela, M., Lehtimaki, T., & Keltikangas-Jarvinen, L. (2007). The influence of urban/rural residency on depressive symptoms is moderated by the serotonin receptor 2A gene. American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics, 144B(7), 918-922. * Jokela, M., Räikkönen, K., Lehtimäki, T., Rontu, R., & Keltikangas-Järvinen, L. (2007). Tryptophan hydroxylase 1 gene (TPH1) moderates the influence of social support on depressive symptoms in adults. Journal of Affective Disorders, 100(1-3), 191-197. * Bakermans-Kranenburg, M. J., & van IJzendoorn, M. H. (2006). Gene-environment interaction of the dopamine D4 receptor (DRD4) and observed maternal insensitivity predicting externalizing behavior in preschoolers. Developmental Psychobiology, 48(5), 406-409. * Mills-Koonce, W. R., Proper, C. B., Gariepy, J. L., Blair, C., Garrett-Peters, P., & Cox, M. J. (2007). Bidirectional genetic and environmental influences on mother and child behavior: the family system as the unit of analyses. Development and Psychopathology, 19(4), 1073-1087. * Kim-Cohen, J., Caspi, A., Taylor, A., Williams, B., Newcombe, R., Craig, I. W., et al. (2006). MAOA, maltreatment, and gene-environment interaction predicting children's mental health: new evidence and a meta-analysis. Molecular Psychiatry, 11(10), 903-913. * Caspi, A., Moffitt, T. E., Cannon, M., McClay, J., Murray, R., Harrington, H., et al. (2005). Moderation of the effect of adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-O-methyltransferase gene: longitudinal evidence of a gene X environment interaction. Biological Psychiatry, 57(10), 1117-1127. * Boyce, W. T., Chesney, M., Alkon, A., Tschann, J. M., Adams, S., Chesterman, B., et al. (1995). Psychobiologic reactivity to stress and childhood respiratory illnesses: results of two prospective studies. Psychosomatic Medicine, 57(5), 411-422. * Gannon, L., Banks, J., Shelton, D., & Luchetta, T. (1989). The mediating effects of psychophysiological reactivity and recovery on the relationship between environmental stress and illness. Journal of Psychosomatic Research, 33(2), 167-175. * El-Sheikh, M., Keller, P. S., & Erath, S. A. (2007). Marital conflict and risk for child maladjustment over time: skin conductance level reactivity as a vulnerability factor. Journal of Abnormal Child Psychology, 35(5), 715-727. * El-Sheikh, M., Harger, J., & Whitson, S. M. (2001). Exposure to interparental conflict and children's adjustment and physical health: the moderating role of vagal tone. Child Development, 72(6), 1617-1636. * Pluess, M., & Belsky, J. (2009). Differential Susceptibility to Parenting and Quality Child Care. Developmental Psychology. * Kochanska, G., Aksan, N., & Joy, M. E. (2007). Children's fearfulness as a moderator of parenting in early socialization: Two longitudinal studies. Developmental Psychology, 43(1), 222-237. * Lengua, L. J. (2008). Anxiousness, frustration, and effortful control as moderators of the relation between parenting and adjustment in middle-childhood. Social Development, 17(3), 554-577. * Aron, E. N., Aron, A., & Davies, K. M. (2005). Adult shyness: the interaction of temperamental sensitivity and an adverse childhood environment. Personality and Social Psychology Bulletin, 31(2), 181-197. Category:Abnormal psychology [psychology Category:Psychological theories